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INTRODUCTION

Although uncommon, significant hemorrhage, coagulopathy, and need for transfusion are encountered by every practicing obstetrician. Prevention is obviously superior to treatment. By understanding the pathophysiology and events that lead to these potentially catastrophic clinical situations, we can respond more rapidly and often prevent them from becoming critical situations. Even with meticulous care, we cannot prevent all such cases. Rapid, decisive, and knowledgeable action on the part of the obstetrician can usually avert an adverse outcome. In this chapter, I cover the areas of clinical disseminated intravascular coagulopathy (DIC) and clinically significant thrombocytopenia. The best form of therapy is aimed at correcting the underlying pathophysiologic problem, as well as treating the acquired or inherent clotting problem. There are many ways to treat these clinical entities. This chapter outlines a practical approach to these patients with these complications.

DISSEMINATED INTRAVASCULAR COAGULOPATHY

Disseminated intravascular coagulopathy (DIC) describes a clinical scenario that can be initiated by many pathologic processes. It is characterized by accelerated formation of fibrin clots with simultaneous breakdown of these same clots. It is, indeed, a consumptive coagulopathy. The body consumes clotting factors faster than they can be produced. This cycle keeps repeating until an intervention stops the cycle or the patient succumbs to hemorrhage. Normally, our body is in a constant balance between fibrin generation and fibrinolysis. When this delicate balance is disturbed and the coagulation cascade and fibrinolytic systems go unchecked, DIC can result. DIC may arise from massive activation of the coagulation system that overwhelms endogenous control mechanisms. This is usually the result of activation of the intrinsic clotting system. DIC, however, may be initiated by exposure of blood to tissue factor, which triggers activation of the factor VII and the extrinsic clotting system. This may be the result of trauma or endotoxins damaging tissue. Also, proteolytic enzyme release may trigger DIC and can occur in events such as placental abruption. This critical clinical picture, in other words, can have many etiologies that manifest similarly. For truly effective treatment, one must rapidly determine the etiology while initiating therapy.

Etiology

The most common obstetric causes of DIC are listed in Table 4-1. The most common underlying cause of mild DIC encountered by the obstetrician is probably underestimation of blood loss at the time of vaginal or cesarean delivery with inadequate replacement by crystalloid or colloid. In these cases, vasospasm occurs with resultant endothelial damage and initiation of DIC. Also, in these instances, hypotension occurs, which results in decreased tissue perfusion leading to local hypoxia and tissue acidosis, which further exacerbates DIC by causing tissue release of cytokines. By keeping the patient’s volume replete, DIC can often be avoided, even in the presence of profound anemia.